Abstract
Advancement of biomedical applications of carbonaceous nanomaterials is hampered by their biopersistence and pro-inflammatory action in vivo. Here, we used myeloperoxidase knockout B6.129X1-MPO (MPO k/o) mice and showed that oxidation and clearance of single walled carbon nanotubes (SWCNT) from the lungs of these animals after pharyngeal aspiration was markedly less effective whereas the inflammatory response was more robust than in wild-type C57Bl/6 mice. Our results provide direct evidence for the participation of MPO - one of the key-orchestrators of inflammatory response - in the in vivo pulmonary oxidative biodegradation of SWCNT and suggest new ways to control the biopersistence of nanomaterials through genetic or pharmacological manipulations.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Bronchoalveolar Lavage Fluid / cytology
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Chemokine CCL2 / metabolism
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Female
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Fibrosis / chemically induced
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Fibrosis / metabolism
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Interleukin-6 / metabolism
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Lung / drug effects*
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Lung / metabolism
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Lung / pathology
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Mice
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Mice, 129 Strain
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Mice, Inbred C57BL
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Mice, Knockout
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Microscopy, Electron, Transmission
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Microscopy, Fluorescence
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Nanotubes, Carbon / toxicity*
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Nanotubes, Carbon / ultrastructure
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Neutrophils / drug effects
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Neutrophils / metabolism
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Oxidation-Reduction
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Peroxidase / deficiency*
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Peroxidase / genetics
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Pneumonia / chemically induced
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Pneumonia / metabolism
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Spectrum Analysis, Raman
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Tumor Necrosis Factor-alpha / metabolism
Substances
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Ccl2 protein, mouse
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Chemokine CCL2
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Interleukin-6
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Nanotubes, Carbon
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Tumor Necrosis Factor-alpha
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Peroxidase